Complications of Myocardial Infarction

Left Ventricular (LV) Thrombus

  • LV thrombus is usually seen in patients presenting with large anterior STEMIs
    • Late presentation is an important risk factor
  • LV thrombus results from the “perfect storm” of factors contributing to “Virchow’s Triad:”
    • LV wall akinesis/dyskinesia resulting in stagnant blood flow
    • Pro-coagulative state
    • Ischemia resulting in inflammation 
  • The incidence of LV thrombus is about 5-7% in anterior MI.
    • (Number may be smaller with modern reperfusion times)
  • Imaging options:
    • Echo (most commonly used)
    • CT or MRI.
  • LV thrombus forms 12-72 hours after MI.
    • Imaging too early in the MI course may not identify an LV thrombus

Treatment of LV Thrombus

  • The most dreaded complication of LV thrombus is stroke.
  • Anticoagulation
    • Vitamin K antagonists (VKAs)
    • DOACs are available, but only used if VKA-intolerant (no clinical trials available, case reports only)
  • Primary prevention in anterior MI
    •  CCS 2018 – No routine anticoagulation (citing poor evidence and high risk of bleeding)
    • AHA 2013 – Class IIB indication for anticoagulation
  • Generally treat with anticoagulation for 3-6 months, and repeat echo to reassess whether the LV thrombus has resolved.

CCS 2018 Heart Failure Guidelines
  • We recommend against routine anticoagulation after large anterior MI and low EF, in the absence of intracardiac thrombus or other indications for anticoagulation (Weak Recommendation; Low-Quality Evidence).
AHA 2013 STEMI Guidelines
  • Anticoagulant therapy may be considered for patients with STEMI and anterior apical akinesis or dyskinesis. (Class IIB) (Level of Evidence: C)
    (Duration: 3 months.  INR 2.0-2.5 if used with DAPT)

Left Ventricular Aneurysm and Pseudoaneurysm

  • Left ventricular aneurysm
    • Result of thinning of the myocardium
    • Identified by a large neck
    • Low risk of rupture
    • Persistent ST elevation on EKG
  • Left ventricular pseudoaneurysm
    • Cardiac myocardial rupture that is contained by the pericardium
    • Very narrow neck
    • High risk for rupture → increased mortality

Right Ventricular (RV) Infarct

  • Complication of inferior STEMIs
  • Loss of RV contractility to maintain forward flow leads to LV underfilling (reduced preload), reduced cardiac output, and hypotension.
    • Drugs that further reduce preload such as nitrates and diuretics can worsen cardiac output leading to worsening hypotension and shock.
  • The RV is supplied mostly by the RV branch of the RCA. A proximal RCA lesion can compromise the RV branch. 
  • Early recognition and diagnosis of an RV infarcts is important.

EKG Findings in RV Infarct

  • Indirect evidence of RV infarction:
    • ST elevation in lead III > Lead II (Suggests RCA occlusion)
    • ST elevation in V1 (Remember: V1 is closest to the RV on a typical 12-lead EKG).
    • ST elevation in V1 but ST depression in V2 (Suggestive of RV infarct).
  • Direct evidence of RV infarction:
    • ST elevation in V4R (V4 Reverse) (15-lead EKG is required). V4R puts a lead directly over the RV.
    • Remember only 0.5mm of ST elevation is required to be considered positive in V4R.

Cath

  • RCA lesions are most common reason for RV infarct as the RV branch is supplied by the RCA.
  • Usually very proximal lesions.
Inferior STEMI with RV infarct

Echocardiogram

  • Can be useful in assessing the severity of an RV infarct
    1. Visual qualitative assessment 
    2. TAPSE (Tricuspid Annular Plane Systolic Excursion) is a validated tool to assess RV function
      • Involves am M-mode at the base of the RV to assess tricuspid annular motion
      • Normal ≥ 1.7 cm
      • TAPSE has been validated as a predictor of heart failure and survival
    3. Tissue Doppler
      • Systolic excursion (S’) of < 9.5 cm/sec is suggestive of RV dysfunction

RV Infarct on ECHO

Management

  • Revascularization
    • Even after revascularization, the right ventricle may take some time to recover.
  • Hypotension Management
    • The main hemodynamic problem resulting from an RV infarction is reduced LV preload, which causes reduced cardiac output/shock and hypotension.
    • Avoid therapies that further reduce preload (nitrates, narcotics, propofol, etc.)
    • Use therapies to improve preload (IV fluids, vasopressors)
  • Dobutamine
    • Improves RV stroke volume, and improves RV afterload by reducing pulmonary vascular resistance
    • Ideally used after revascularization, as inotropes can cause complications during acute MI (arrhythmias, increase in infarct size, etc.)
 

Heart Block

Inferior infarct-related heart block:

  • Usually RCA, rarely can be circumflex
  • Heart block associated with high-vagal tone Bezold-Jarisch reflex or rarely from AV node ischemia
  • Often transient and can be treated with atropine
  • Pacemaker should generally be avoided due to risk of RV perforation (can be placed in extreme circumstances)

Anterior infarct-related heart block:

  • Usually related to extensive infarct and damage to the conduction system in the septum
  • Complete heart block often preceded by RBBB + LAFB
  • Temporary/permanent pacemaker more likely to be required; usually see more distal conduction disease like Mobitz 2, third degree heart block, or alternating bundle branch blocks
Inferior STEMI with Wenkebach

Ventricular Septal Defect

  • A very uncommon complication of acute MI.
  • Typically seen in late-presenting patients who have not been revascularized. They are often female, older patients, and have no history of MI/Angina prior to presentation (less collaterals).
  • Often have poor prognosis.

Types

  1. Anterior Infarct often located at the apical ventricular septal.
  2. Inferior Infarct often located at the inferobasal ventricular septum. Usually a worse prognosis.

Clinical Features

  • Prominent pan-systolic murmur at left lower sternal border often associated with a thrill.
  • Signs of right sided heart failure, pulmonary edema or shock.
  • Echo helps confirm evidence of a VSD with left to right shunt as well as complications such as RV failure.

Management

  • Hemodynamic support with ionotropes, afterload reduction with nitroprusside and can consider IABP for mechanical support as bridge to surgery
  • Surgical closure or percutaneous options

Myocardial Rupture

  • Uncommon complication but very high mortality.
  • The risk factors are similar to VSDs: patients are often older, late-presenting, female, first presentation MI (lack of collaterals)
  • Patients can have sudden PEA arrest from cardiac tamponade
  • Myocardial rupture is typically preceded by pain similar to the patient’s initial presentation
  • Hypertension, excessive straining, coughing, or vomiting may be triggers

Management

  • Cardiac Arrest → Standard ACLS plus pericardiocentesis
  • Hemodynamic compromise → Fluids, dobutamine/pressors, pericardiocentesis
  • Traditionally, pericardiocentesis was discouraged in patients with myocardial rupture due to concern of worsening hemorrhage into the pericardial space. However, pericardiocentesis (with removal of only 10-50 mL) is still sometimes performed in patients with extreme hemodynamic instability to improve hemodynamics until definitive surgical management is delivered.
  • Surgical consultation is a must. Teflon or pericardial patch can be performed on the epicardium to stabilize the rupture.

Papillary Muscle Rupture

  • Presentation:
    • Pulmonary edema
    • Hypotension
    • Shock
    • Murmur: may not be very loud because of rapid equalization of pressures across the mitral valve, but patients will have severe MR
  • Posteromedial papillary muscle
    • Most common
    • Single blood supply PDA
  • Anterolateral papillary muscle
    • Dual blood supply from the LAD and circumflex artery
  • Treatment
    • Inotropes
    • IABP
    • URGENT surgical consult

Transthoractic Echo

Transesophageal Echo

References

  • Figueras J, Cortadellas J, Soler-Soler J Left ventricular free wall rupture: clinical presentation and management

Contributors

  • Primary Author: Dr. Daniel Durocher (MD FRCPC)
  • Reviewers:
    • Dr. Pavel Antiperovitch (MD, FRCPC)
    • Perri Deacon (medical student)
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